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Biomedical subjects

L Share

Publications and source records attributed to L Share.

At least 55 records · Page 3Linked to original sources
PubMed1990

Sexual dimorphism in vasopressin and cardiovascular response to hemorrhage in the rat.

There is evidence for sex-related differences in the cardiovascular actions of vasopressin. Furthermore, receptors for the gonadal steroid hormones are located in centers in the brain involved in the control of vasopressin release and in cardiovascular regulation. We have, therefore, examined the effects of hemorrhage on mean arterial blood pressure, the plasma vasopressin concentration, and plasma renin concentration in conscious male and female rats. In preliminary experiments, no differences were found in blood and plasma volumes with respect to either sex or phase of the estrous cycle. In separate experiments, rats were subjected to two hemorrhages of 10% of blood volume, separated by an interval of 15 minutes. There were no substantial gender- or cycle-related differences in the ability of hemorrhaged rats to maintain mean arterial blood pressure or increase plasma renin concentration. The increase in plasma vasopressin concentration was greater in proestrous females than in males after the first hemorrhage and in diestrous, proestrous, and metestrous females than in males after the second hemorrhage. Pretreatment with a V1-receptor antagonist was without statistically significant effect on the mean arterial blood pressure responses in males, but it impaired blood pressure compensation in females. There are, then, gender- and cycle-related differences in vasopressin responses to hemorrhage, and vasopressin appears particularly important for blood pressure compensation to hemorrhage in female rats.

Animals↗
PubMed1990

Nonosmotic stimuli alter osmoregulation in patients with spinal cord injury.

Studies on two quadriplegic patients who developed severe hyponatremia during episodes of acute respiratory distress were performed to determine whether differences in osmoregulation of vasopressin release could be identified in these patients compared to other quadriplegic subjects previously studied in a similar manner. Both patients were clinically stable and normonatremic, with no signs or symptoms of respiratory distress, when the studies were performed. However, both exhibited evidence of hemodynamic instability in the sitting posture. Linear regression analysis of the plasma vasopressin/plasma osmolality (Pavp:Posm) relationship during infusions of 0.85 M sodium chloride showed no significant differences in either the slope (sensitivity) or abscissal intercept (osmotic threshold) of this relationship compared to that of other quadriplegic subjects when the patients were supine. In contrast, when the patients were studied in the sitting posture there was a marked shift in the relationship of Pavp:Posm indicative of increased sensitivity and reduced osmotic threshold for vasopressin release. The slopes of the Pavp:Posm relationships were 0.249 and 0.178 for the two patients, respectively, compared to 0.092 +/- 0.03 ( +/- SD) for previously studied quadriplegic subjects. Oral water-loading studies performed on one patient revealed marked impairment of urine-diluting ability and free water clearance in the sitting posture compared with observations in similar studies performed when the patient was supine. Impairment of renal water excretion could not be attributed to an effect of vasopressin, which was reduced to unquantifiable levels by water loading. These studies have shown that hemodynamic stress related to autonomic dysfunction in quadriplegic patients may result in marked alteration of osmoregulation of vasopressin release in more severely affected individuals. Such altered osmoregulation, which may also be associated with vasopressin-independent impairment of renal water excretion in the sitting posture, may be a predisposing factor in the development of hyponatremia, especially in the presence of other potent nonosmotic stimuli.

Aged↗
PubMed1989

Role of brain acetylcholine in vasopressin release during osmotic stimulation and hemorrhage.

There is considerable evidence to suggest that there is a cholinergic link in the neural control of vasopressin release, but the precise role for this link has not been adequately demonstrated in the intact animal. We have, therefore, examined in conscious unrestrained rats the effects of central cholinergic blockade on the stimulation of vasopressin release by increased plasma osmotality (iv infusion of 2.5 M NaCl at 0.1 mg/kg body weight.min for 30 min) and by decreased blood volume (2 successive hemorrhages of 10% of blood volume each). The vasopressin responses to these stimuli were unaffected by either intracerebroventricular (icv) atropine (10 micrograms; muscarinic blockade) or icv hexamethonium (10 micrograms; nicotinic blockade) in doses which block the vasopressin responses to icv cholinergic agonists. The implications of these findings are discussed.

Acetylcholine↗
PubMed1989

Pressor responses to vasopressin in pigs and sheep with DOCA hypertension.

Pressor responses to vasopressin were determined in pigs and sheep during three experimental periods: 1) before deoxycorticosterone acetate (DOCA) treatment, 2) 21 days after DOCA implantation (100 mg/kg) when a stable hypertension had developed, and 3) after reversal of the hypertension by removing the implant in the sheep or by decreasing the dietary sodium intake in the pigs. The infusion of lysine (LVP) or arginine (AVP) vasopressin into pigs and sheep, respectively, resulted in dose-dependent increases in plasma vasopressin concentration. The levels of plasma LVP or AVP achieved by these infusions were not altered in any of the experimental periods. The administration of vasopressin resulted in dose-dependent increases in mean arterial blood pressure. However, pigs required five times more LVP than sheep required AVP to achieve similar pressor responses. The pressor responsiveness to vasopressin was attenuated when either species was made hypertensive. This effect was reversed when normal blood pressure was restored by reducing sodium intake in the pigs or by removing the DOCA implant from the sheep. These data establish that an increased pressor response to vasopressin does not contribute to DOCA hypertension in pigs or sheep.

Animals↗
PubMed1989

Osmotic control of vasopressin in male and female rats.

To examine the osmotic control of vasopressin release, hypertonic saline was infused in conscious unrestrained male rats and female rats in each phase of the estrous cycle. The progressive increase in plasma osmolality was accompanied by a progressive increase in the plasma vasopressin concentration, but the magnitude of the former was smaller in metestrus than in other phases of the cycle and in males (P less than 0.01). The osmotic threshold for vasopressin release was higher in males than in females in each phase of the estrous cycle (P less than 0.05 to P less than 0.01), but the sensitivity of the osmotic control of vasopressin release was similar in male and female rats. Although the pressor response to hypertonic saline was greater in estrous females than in the other females (P less than 0.05 to P less than 0.01), the reduction in blood pressure, after a V1 antagonist 30 min after starting the hypertonic saline infusion, was similar in males and females. Thus there are gender-related differences in the osmotic control of vasopressin release and, in females, cycle-dependent differences in the cardiovascular responses to hypertonic saline.

Animals↗
PubMed1989

Sex differences in central adrenergic control of vasopressin release.

Central adrenoreceptor-mediated regulation of vasopressin secretion and cardiovascular function was studied in male rats and female rats in specific estrous cycle phases. In conscious, unrestrained rats with intracerebroventricular (icv) cannulas and femoral artery and vein catheters, plasma arginine vasopressin concentration (PAVP), mean arterial blood pressure (MABP), and heart rate (HR) were determined before and 5 and 15 min after icv injection of 10 micrograms norepinephrine or 50 micrograms phenylephrine. Norepinephrine (icv) increased PAVP in proestrus and metestrus four and three times (P less than 0.01 and 0.05, respectively) more than in males. Norepinephrine induced similar MABP elevations (P less than 0.01) in males and females in all cycle phases; HR decreased only in proestrus, estrus, and metestrus (P less than 0.01). The increase in PAVP after icv phenylephrine was four and three times greater in proestrous and diestrous females (P less than 0.01 and 0.05, respectively) than in males. The proestrous MABP rise was three times that in males (P less than 0.05); HR decreased similarly in diestrus, proestrus, and males. These results suggest gonadal steroid hormones influence adrenoreceptor-mediated control of vasopressin secretion, MABP, and HR.

Animals↗
PubMed1989

Increased urinary clearance of lysine vasopressin in the deoxycorticosterone acetate-hypertensive pig.

We have previously reported an increased urinary excretion of vasopressin without a rise in circulating levels of this hormone in the deoxycorticosterone acetate (DOCA)-hypertensive pig (DH). The present study was designed to characterize the renal handling of vasopressin in DH that might account for this paradox. DOCA hypertension was produced in seven domestic female pigs by means of subcutaneous implants of Silastic rubber impregnated with DOCA. Thirty days after DOCA implantation, urinary clearances of inulin, para-aminohippurate (PAH), and vasopressin were measured in the conscious animals during infusion of a 5% dextrose solution, first without and then with lysine vasopressin. Subsequent to this study, four of the pigs were placed on a low-sodium (10 meq/kg food) diet for 4 wk. At the end of this period, the clearances were again evaluated. We observed an increased urinary vasopressin clearance (CLVP) in the DH associated with an increased urinary flow but without significant changes in the clearances of inulin or PAH. Dietary sodium restrictions reversed the hypertension and the increased urinary flow and returned the CLVP to normotensive levels. These results indicate that the increased urinary excretion of vasopressin in DH is because of an increased urinary clearance of this hormone. This increased urinary CLVP is the consequence of the high urine flow in these pigs.

Animals↗
PubMed1989

Effect on vasopressin release of microinjection of angiotensin II into the paraventricular nucleus of conscious rats.

We have studied in conscious unrestrained rats the role of angiotensin II receptors in the paraventricular nucleus (PVN) in the control of vasopressin secretion under basal conditions and after 24 h of water deprivation. In euhydrated rats, the microinjection rostral to the PVN of 1 and 5 ng of angiotensin II produced a transient, dose-dependent increase in the plasma vasopressin concentration. There was also a transient, but not dose-dependent, rise in mean arterial blood pressure (MABP), without a change in heart rate. However, the microinjection of angiotensin II into the PVN and sites caudal to it was without effect on the measured variables. In dehydrated rats, on the other hand, microinjection of 5 ng angiotensin II, both into the PVN and rostral to it, resulted in a prolonged increase in the plasma vasopressin concentration. The response from the rostral site was more rapid and was associated with an increased MABP. These findings suggest that angiotensin II receptors rostral to the PVN may participate in the control of vasopressin release in both euhydrated and dehydrated states, whereas angiotensin II receptors in the PVN are effective only following dehydration.

Angiotensin II↗
PubMed1989

Vasopressin in rats with genetic and streptozocin-induced diabetes.

Rats were administered streptozocin (STZ; 50 or 75 mg/kg i.v., tail vein) or vehicle. Approximately 2 wk later, venous and arterial catheters was implanted for subsequent (24 h later) vasopressin, electrolyte, and hemodynamic measurements. STZ-induced diabetic (STZ-D) rats demonstrated a dose-dependent increase in the plasma glucose concentration, plasma osmolality, and plasma vasopressin concentration. Mean arterial blood pressure (MABP) was unchanged, but heart rate was reduced. Diabetes-prone BB rats, maintained on or withdrawn from insulin treatment for 24-48 h, and diabetes-resistant rats were instrumented and studied as above. Spontaneous-diabetes-prone rats demonstrated increase in plasma glucose concentration and plasma osmolality similar to STZ-D rats but had significantly greater plasma vasopressin concentrations. The significant decrease in MABP observed in these animals probably contributed to the enhanced vasopressin response. We conclude that both osmotic and cardiovascular parameters play important roles in vasopressin secretion in diabetic rats.

Animals↗
PubMed1989

Gonadectomy abolishes the sexual dimorphism in DOC-salt hypertension in the rat.

Following our previous report that development of DOC-salt hypertension is attenuated in female rats, we have now determined the effects of gonadectomy on the pathogenesis of this model of hypertension. Male and female rats were gonadectomized at age three weeks, and the DOC-salt protocol was initiated two weeks later and continued for three weeks. In intact rats, hypertension developed more rapidly and to a higher level in males than in females. By contrast, in gonadectomized rats, there was no sex difference in blood pressure because the development of hypertension was attenuated in males and exacerbated in females. None of these differences could be attributed to differences in either saline consumption or vasopressin release since no differences were found among the groups for either variable. Although the underlying mechanisms are uncertain, our results clearly show that the gonadal hormones affect the development of DOC-salt hypertension in the rat.

Animals↗
PubMed1988

Vasopressin: sexual dimorphism in secretion, cardiovascular actions and hypertension.

We have investigated the issue of sexual dimorphism in the secretion of vasopressin, its pressor action, and the development of deoxycorticosterone (DOC)-salt hypertension. In normal human subjects on controlled salt intake, the basal secretion of vasopressin, indicated by plasma vasopressin levels and urinary excretion of vasopressin, was higher in men than in women and in blacks than in whites. Basal vasopressin secretion also was higher in male than in female rats. This effect was not associated with a difference in the metabolic clearance of the hormone. The sex-related difference in vasopressin release in rats was abolished by gonadectomy and restored by treatment of males with testosterone and females with ovarian hormones. The pressor responsiveness to vasopressin was higher in male than in randomly cycling female rats. Finally, DOC-salt hypertension, which is dependent on vasopressin, developed more rapidly in male than in female rats. Although there was no sex-related difference in the extent to which plasma vasopressin levels were elevated, pressor responsiveness to vasopressin was greater and baroreflex sensitivity was attenuated to a lesser extent in hypertensive males than in hypertensive females. Thus, it seems likely that gonadal hormones play a significant role in cardiovascular regulation.

Animals↗
PubMed1988

Pressor responsiveness to and secretion of vasopressin during the estrous cycle.

Previously, we observed a sexual dimorphism of the pressor responsiveness to vasopressin in the rat. We have now determined that the pressor action of vasopressin is influenced by the phase of the estrous cycle. Conscious unrestrained male and female rats were given graded intravenous 30-min infusions of vasopressin. The pressor responses of male and estrous female rats were similar, whereas the pressor responses of diestrous, proestrous, and metestrous females were substantially (P less than 0.01) attenuated. This effect could not be attributed to differences in baroreflex sensitivity, which was unaffected by the sex of the rat or phase of the estrous cycle. Baroreflex sensitivity was assessed by the slope of the relationship between changes in heart rate and mean arterial blood pressure in response to graded injections of phenylephrine and nitroprusside. The basal plasma vasopressin concentration was higher (P less than 0.05) in male than in female rats in each phase of the estrous cycle. This was due to a difference in vasopressin release, since there were no sex-related differences in the metabolic clearance rate of vasopressin. These findings suggest that the gonadal hormones influence the cardiovascular actions of vasopressin and its secretion.

Angiotensin II↗
PubMed1988

Sex difference in pressor responsiveness to vasopressin and baroreflex function in DOC-salt hypertensive rats.

This study was undertaken to investigate further the possible role of vasopressin in the sexual dimorphism of deoxycorticosterone (DOC)-salt hypertension. The study was carried out 3 weeks after initiating treatment with DOC and salt in uninephrectomized male and female rats. Mean arterial pressure (MAP) was lower in female than in male DOC-salt hypertensive rats (177 +/- 7 versus 198 +/- 4 mmHg; P less than 0.01). Mean arterial pressure did not differ between male and female normotensive control rats. Increases in MAP in response to graded i.v. infusions of vasopressin were markedly attenuated in female normotensive and hypertensive rats, but there was no sex difference in pressor responses to i.v. phenylephrine. Baroreflex sensitivity was reduced in both male and female DOC-salt rats, but to a greater extent in males (P less than 0.01). Diminished pressor responsiveness to vasopressin and a smaller impairment of baroreflex sensitivity may contribute to the reduced development of DOC-salt hypertension in female rats.

Animals↗
PubMed1987

Vasopressin responses to asphyxia and hemorrhage in newborn pigs.

Vasopressin may be important in maintenance of arterial pressure and redistribution of cardiac output in hypotensive and asphyxiated newborns. We used chronically instrumented, unanesthetized, 4-day-old pigs to investigate the effects of hypotensive hemorrhage and asphyxia on plasma vasopressin concentration and to determine the effects of cyclooxygenase inhibition on these responses. Asphyxia [arterial O2 partial pressure (PaO2) = 40-50 Torr, arterial CO2 partial pressure (PaCO2) = 60-80 Torr) increases plasma lysine vasopressin (LVP) from 2.2 +/- 0.8 to 52.4 +/- 15.0 microU/ml. Neither the baseline nor stimulated plasma LVP was affected by indomethacin (5 mg/kg) or meclofenamate (5 mg/kg). Hemorrhage (30 ml/kg) increased plasma LVP from 2.8 +/- 0.8 to 163.4 +/- 28.1 (20 min) and 135.1 +/- 18.5 microU/ml (60 min). The effects of vehicle and indomethacin (5 mg/kg) 20 min after hemorrhage on plasma LVP 60 min after hemorrhage were not different. Changes in plasma vasopressin caused by asphyxia and hemorrhage in the unanesthetized newborn pig are similar to the responses observed in adults of other species. This study does not suggest that prostanoids are involved in these responses in newborn pigs.

Animals↗
PubMed1987

Adrenergic mediation of vasopressin secretion in newborn pigs.

Effects of inhibition of alpha 1-(prazosin) and alpha 2-(yohimbine) adrenoreceptors on plasma lysine vasopressin concentration during normotension and hemorrhagic hypotension were studied in unanesthetized newborn pigs. During the normotensive period, treatment with prazosin and yohimbine both increased plasma lysine vasopressin concentration (vehicle = 3.4 +/- 1.21 microU/ml; prazosin = 35.8 +/- 10.8 microU/ml; and yohimbine = 20.1 +/- 9.5 microU/ml). Prazosin caused a decline in arterial pressure (vehicle = 60 +/- 6 mmHg; prazosin = 49 +/- 5 mmHg), which may account for the increase in plasma lysine vasopressin concentration, whereas yohimbine increased arterial pressure (73 +/- 3 mmHg). On hemorrhage to equivalent arterial pressure, plasma lysine vasopressin concentration increased to similar levels in vehicle- (110.3 +/- 28.7 microU/ml) and prazosin-treated (92.6 +/- 14.2 microU/ml) piglets. In contrast, on hemorrhage of yohimbine-treated piglets, the increase in plasma lysine vasopressin concentration was augmented remarkably (527.0 +/- 103.2 microU/ml) in comparison to the other groups. We conclude that, in unanesthetized newborn pigs, treatment with the alpha 2-adrenoreceptor antagonist yohimbine increased plasma lysine vasopressin concentration and markedly accentuated the vasopressin response to hemorrhage. An alpha 2-adrenergic receptor-mediated mechanism appears to be an important inhibitory component in the vasopressin secretory system of the newborn pig.

Animals↗
PubMed1987

Sex difference in the development of deoxycorticosterone-salt hypertension in the rat.

To investigate a possible sex difference in the development of deoxycorticosterone (DOC)-salt hypertension in rats, systolic blood pressure was measured over 6 weeks in unilaterally nephrectomized male and female rats with or without DOC-salt treatment. Throughout the treatment, systolic blood pressure was significantly lower in female than in male DOC-salt rats (at the end of the sixth week: 190 +/- 8 vs 163 +/- 7 mm Hg, p less than 0.05). The difference in blood pressure was also confirmed by the direct measurement of mean arterial pressure at the end of the experiment. The 24-hour urinary excretion of vasopressin was significantly higher in male control rats than in female control rats; however, no difference was observed between male and female DOC-salt rats, in which the urinary excretion of vasopressin was four to five times higher than in control rats. The plasma vasopressin concentration was higher in DOC-salt rats, but there were no differences between sexes. There were no differences in the metabolic clearance rate of vasopressin among the four groups of rats. This indicates that the elevated plasma vasopressin concentration in DOC-salt hypertensive rats is due to increased release of the hormone, rather than to impaired metabolism. Thus, although vasopressin plays a pivotal role in the pathogenesis of DOC-salt hypertension, the sexual dimorphism in this form of hypertension cannot be attributed to differences in the secretion, metabolism, or plasma concentration of vasopressin.

Animals↗
PubMed1986

High potassium intake increases the plasma concentration and urinary excretion of vasopressin in the rat.

The effect of alterations of dietary potassium intake on the plasma concentration and the urinary excretion of vasopressin was studied in male rats. Ingestion of a high potassium diet resulted in increases in the plasma concentrations of potassium and vasopressin, systolic blood pressure, urine flow, and urinary vasopressin excretion. Ingestion of a low potassium diet had little effect on the plasma vasopressin concentration and systolic blood pressure but caused decreases in the plasma potassium concentration and urinary vasopressin excretion. The results indicate that physiological changes in the plasma potassium concentration or some other consequence of altered dietary potassium intake can affect vasopressin release and excretion.

Animals↗